Cancers,
Journal Year:
2024,
Volume and Issue:
16(1), P. 234 - 234
Published: Jan. 4, 2024
Metastasis-associated
lung
adenocarcinoma
transcript-1
(MALAT-1)
is
a
long
intergenic
non-coding
RNA
(lncRNA)
located
on
chr11q13.
It
overexpressed
in
several
cancers
and
controls
gene
expression
through
chromatin
modification,
transcriptional
regulation,
post-transcriptional
regulation.
Importantly,
MALAT-1
stimulates
cell
proliferation,
migration,
metastasis
serves
vital
role
driving
the
epithelial-to-mesenchymal
transition
(EMT),
subsequently
acquiring
cancer
stem
cell-like
properties
developing
drug
resistance.
modulates
EMT
by
interacting
with
various
intracellular
signaling
pathways,
notably
phosphoinositide
3-kinase
(PI3K)/Akt
Wnt/β-catenin
pathways.
also
behaves
like
sponge
for
microRNAs,
preventing
their
interaction
target
genes
promoting
EMT.
In
addition,
we
have
used
bioinformatics
online
tools
to
highlight
disparities
of
between
normal
samples
using
data
from
The
Cancer
Genome
Atlas
(TCGA).
Furthermore,
intricate
interplay
essential
targets
progression
renders
it
good
candidate
therapeutic
interventions.
Several
innovative
approaches
been
exploited
MALAT-1,
such
as
short
hairpin
RNAs
(shRNAs),
antisense
oligonucleotides
(ASOs),
natural
products.
This
review
emphasizes
modulating
metastasis,
stemness,
chemoresistance
different
cancers.
Nature Communications,
Journal Year:
2022,
Volume and Issue:
13(1)
Published: May 13, 2022
Abstract
Mass-spectrometry-based
proteomic
data
on
human
tumors—combined
with
corresponding
multi-omics
data—present
opportunities
for
systematic
and
pan-cancer
proteogenomic
analyses.
Here,
we
assemble
a
compendium
dataset
of
proteomics
2002
primary
tumors
from
14
cancer
types
17
studies.
Protein
expression
genes
broadly
correlates
mRNA
levels
or
copy
number
alterations
(CNAs)
across
tumors,
but
notable
exceptions.
Based
unsupervised
clustering,
separate
into
11
distinct
proteome-based
subtypes
spanning
multiple
tissue-based
types.
Two
are
enriched
brain
one
subtype
associating
MYC,
Wnt,
Hippo
pathways
high
CNA
burden,
another
metabolic
low
burden.
Somatic
alteration
in
pathway
associates
higher
activity
as
inferred
by
proteome
transcriptome
data.
A
substantial
fraction
cancers
shows
MYC
without
gain
mutations
noncanonical
roles
MYC.
Our
proteogenomics
survey
reveals
the
interplay
between
genome
tumor
lineages.
npj Precision Oncology,
Journal Year:
2023,
Volume and Issue:
7(1)
Published: June 13, 2023
Abstract
Cyclin
dependent
kinases
(CDKs)
are
serine/threonine
that
proposed
as
promising
candidate
targets
for
cancer
treatment.
These
proteins
complexed
with
cyclins
play
a
critical
role
in
cell
cycle
progression.
Most
CDKs
demonstrate
substantially
higher
expression
tissues
compared
normal
and,
according
to
the
TCGA
database,
correlate
survival
rate
multiple
types.
Deregulation
of
CDK1
has
been
shown
be
closely
associated
tumorigenesis.
activation
plays
wide
range
types;
and
phosphorylation
its
many
substrates
greatly
influences
their
function
Enrichment
interacting
Kyoto
Encyclopedia
Genes
Genomes
(KEGG)
pathway
analysis
was
conducted
participate
oncogenic
pathways.
This
abundance
evidence
clearly
supports
target
therapy.
A
number
small
molecules
targeting
or
have
developed
evaluated
preclinical
studies.
Notably,
some
these
also
subjected
human
clinical
trials.
review
evaluates
mechanisms
implications
tumorigenesis
Scientific Reports,
Journal Year:
2024,
Volume and Issue:
14(1)
Published: Oct. 25, 2024
Accumulating
research
showed
that
ENC1
plays
a
critical
role
in
maintaining
the
physiological
functions.
However,
little
is
known
about
its
predicting
prognosis
and
immunotherapy
response
across
cancers.
In
our
results,
compared
to
normal
tissues,
most
cancer
tissues
exhibit
increased
expression.
We
found
common
type
of
genetic
variation
was
gene
mutation.
addition,
positive
correlation
between
CNV
Moreover,
overexpression
positively
correlated
with
poor
clinical
outcomes.
The
GSEA
results
closely
tumor-promoting
biological
functions
also
negatively
associated
infiltration
levels
T
cells,
activated
NK
B
cells.
Most
immunomodulators
are
ENC1.
Further,
we
verified
inhibition
expression
suppressed
proliferation
migration
breast
cancer,
pancreatic
glioma
conclusion,
study
demonstrated
protumorigenic
Additionally,
tumor
microenvironment
features
immune
checkpoint
inhibitors
Overall,
could
serve
as
promising
potential
prognostic
biomarker
various
tumors.
Redox Biology,
Journal Year:
2024,
Volume and Issue:
75, P. 103302 - 103302
Published: Aug. 6, 2024
Mitochondrial
dysfunction
and
metabolic
reprogramming
can
lead
to
the
development
progression
of
hepatocellular
carcinoma
(HCC).
Ferredoxin
1
(FDX1)
is
a
small
mitochondrial
protein
recent
studies
have
shown
that
FDX1
plays
an
important
role
in
tumor
cuproptosis,
but
its
HCC
still
elusive.
In
this
study,
we
aim
investigate
expression
novel
functions
HCC.
Journal of Cellular and Molecular Medicine,
Journal Year:
2024,
Volume and Issue:
28(7), P. 1 - 20
Published: March 20, 2024
Abstract
YARS
is
responsible
for
catalysing
the
binding
of
tyrosine
to
its
cognate
tRNA
and
plays
a
crucial
role
in
basic
biosynthesis.
However,
biological
functions
bladder
cancer
remains
be
proven.
We
analysed
variations
YARS1
expression
survival
using
multiple
data
sets,
including
TCGA‐BLCA,
GSE13507
cancer‐specific
tissue
microarrays.
Furthermore,
we
explored
transcriptome
data.
Our
findings
revealed
noteworthy
correlation
between
immune
infiltration
cancer,
as
determined
XCELL
algorithm
single‐cell
analysis.
In
addition,
employed
TIDE
evaluate
responsiveness
different
cohorts
checkpoint
therapy.
investigated
regulatory
associations
various
aspects
senescence,
ferroptosis
stemness.
Finally,
established
ceRNA
network
that
directly
linked
overall
prognosis,
can
serve
prognostic
biomarker
cancer;
interaction
with
MYC
has
implications
cell
Moreover,
identified
potential
therapeutic
target
cancer.
Cell Division,
Journal Year:
2025,
Volume and Issue:
20(1)
Published: Jan. 17, 2025
Dysregulation
of
SF3A3
has
been
related
to
the
development
many
cancers.
Here,
we
investigated
functional
role
in
hepatocellular
carcinoma
(HCC).
expression
HCC
tissues
and
cell
lines
was
examined
using
RT-qPCR.
Changes
malignant
behavior
cells
after
downregulation
were
assessed
by
EdU,
colony
formation,
flow
cytometry,
wound
healing,
Transwell
invasion
assays.
Multiple
datasets
combined
identify
upstream
modifiers
SF3A3.
The
binding
relationship
between
STIL
FOXM1
explored
co-IP
assay,
effect
on
at
promoter
detected
ChIP-qPCR
assay.
A
xenograft
tumor
model
established
explore
changes
tumors
vivo,
Ki67,
GPC3,
p53
immunohistochemistry.
overexpressed
cells,
or
inhibited
promoting
p53.
An
interaction
regulated
cells.
Knockdown
further
enhanced
anti-tumor
effects
loss
vitro
whereas
overexpression
overturned
impact
vivo.
Our
findings
indicate
that
STIL/FOXM1
expedites
activating
SF3A3,
which
highlights
importance
as
a
promising
prognostic
marker
therapeutic
target
for
HCC.
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: Jan. 25, 2025
Netrin-1
(NTN1)
is
a
laminin-related
secreted
protein
involved
in
axon
guidance
and
cell
migration.
Previous
research
has
established
significant
connection
between
NTN1
nervous
system
development.
In
recent
years,
mounting
evidence
indicates
that
also
plays
crucial
role
tumorigenesis
tumor
progression.
For
instance,
inhibiting
been
shown
to
suppress
growth
epithelial-mesenchymal
transition
(EMT)
characteristics
endometrial
cancer.
To
further
elucidate
the
influence
of
genes
on
tumors,
we
utilized
variety
machine
learning
techniques
found
strongly
linked
multiple
cancer
types,
suggesting
it
as
potential
therapeutic
target.
This
study
aimed
pan-cancer
using
multi-omics
data
explore
its
prognostic
biomarker
SKCM.
Analysis
TCGA,
GTEx,
UALCAN
databases
revealed
differences
expression
at
both
mRNA
levels.
Prognostic
value
was
evaluated
through
univariate
Cox
regression
Kaplan–Meier
methods.
Mutation
methylation
analyses
were
conducted
cBioPortal
SMART
databases.
We
identified
interacting
with
correlated
STRING
GEPIA2,
respectively.
Subsequently,
performed
GO
KEGG
enrichment
analyses.
The
results
suggested
might
be
biological
processes
pathways
related
development
progression,
including
adhesion,
guidance,
immune
response,
various
signaling
pathways.
then
explored
correlation
infiltration
well
immunotherapy
ESTIMATE
package,
TIMER2.0,
TISIDB,
TIDE,
TIMSO,
TCIA.
relationship
heterogeneity,
stemness,
DNA
methyltransferases,
MMR
examined.
Lastly,
constructed
nomogram
based
SKCM
investigated
association
drug
sensitivity.
significantly
associated
infiltration,
molecular
subtypes,
clinicopathological
features
cancers.
Genetic
analysis
Deep
deletions
most
common
type
alteration.
Additionally,
positive
observed
CNAs
cancers,
showed
correlations
stromal
scores,
specific
populations.
Its
predictive
for
response
comparable
mutational
burden.
Furthermore,
exhibited
methyltransferase
genes,
genes.
SKCM,
an
independent
risk
factor
demonstrated
associations
drugs.
exhibits
substantial
clinical
utility
marker
indicator
across
types.
comprehensive
provides
insights
into
implications
research.
Nature Communications,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: Jan. 29, 2025
Ferroptosis
is
a
form
of
iron-dependent
programmed
cell
death,
which
distinct
from
apoptosis,
necrosis,
and
autophagy.
Mitochondria
play
critical
role
in
initiating
amplifying
ferroptosis
cancer
cells.
Voltage-Dependent
Anion
Channel
1
(VDAC1)
embedded
the
mitochondrial
outer
membrane,
exerts
roles
regulation
ferroptosis.
However,
mechanisms
VDAC1
oligomerization
regulating
are
not
well
elucidated.
Here,
we
identify
that
binding
protein
V-Set
Transmembrane
Domain
Containing
2
Like
(VSTM2L),
mainly
localized
to
mitochondria,
positively
associated
with
prostate
(PCa)
progression,
key
regulator
Moreover,
VSTM2L
knockdown
PCa
cells
enhances
sensitivity
RSL3-induced
Mechanistically,
forms
complex
hexokinase
(HK2),
enhancing
their
affinity
preventing
oligomerization,
thereby
inhibiting
maintaining
mitochondria
homeostasis
vitro
vivo.
Collectively,
our
findings
reveal
pivotal
for
mitochondria-localized
driving
resistance
highlight
its
potential
as
ferroptosis-inducing
therapeutic
target
treatment
PCa.